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Review
. 2022 May 25;23(11):5938.
doi: 10.3390/ijms23115938.

An Overview of Oxidative Stress, Neuroinflammation, and Neurodegenerative Diseases

Daniel Mihai Teleanu  1 , Adelina-Gabriela Niculescu  2 , Iulia Ioana Lungu  2   3 , Crina Ioana Radu  4 , Oana Vladâcenco  1   5 , Eugenia Roza  1   5 , Bogdan Costăchescu  6   7 , Alexandru Mihai Grumezescu  2   8   9 , Raluca Ioana Teleanu  1   5
Affiliations
Review

An Overview of Oxidative Stress, Neuroinflammation, and Neurodegenerative Diseases

Daniel Mihai Teleanu et al. Int J Mol Sci. .

Abstract

Oxidative stress has been linked with a variety of diseases, being involved in the debut and/or progress of several neurodegenerative disorders. This review intends to summarize some of the findings that correlate the overproduction of reactive oxygen species with the pathophysiology of Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis. Oxidative stress was also noted to modify the inflammatory response. Even though oxidative stress and neuroinflammation are two totally different pathological events, they are linked and affect one another. Nonetheless, there are still several mechanisms that need to be understood regarding the onset and the progress of neurodegenerative diseases in order to develop efficient therapies. As antioxidants are a means to alter oxidative stress and slow down the symptoms of these neurodegenerative diseases, the most common antioxidants, enzymatic as well as non-enzymatic, have been mentioned in this paper as therapeutic options for the discussed disorders.

Keywords: antioxidants; neurodegenerative disease; neuroinflammation; reactive oxidative species.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Generally known reactive oxygen species (ROS). Adapted from [13].
Figure 2
Figure 2
Dopamine metabolism and ROS production. Reprinted from an open-access source [21].
Figure 3
Figure 3
Schematic representation of alterations in dopamine, iron, and alfa-synuclein promoting oxidative stress in the substantia nigra pars compacta. Reprinted from an open-access source [21].
Figure 4
Figure 4
The model of motor nerve terminal dysregulation in ALS. (A) Healthy NMJ. (B) Pathological changes in NMJ during early stage of ALS. (C) Pathological changes in NMJ during late stage of ALS. Abbreviations: Ach—acetyl choline, MuSK—muscle-specific kinase, NMJ—neuromuscular junction, ROS—reactive oxygen species, TSC—terminal Schwann. Reprinted from an open-access source [34].
Figure 5
Figure 5
Representation of ROS-induced mitochondrial abnormalities in AD. Reprinted from an open-access source [9].
Figure 6
Figure 6
Mutant HTT (mHTT)-induced mitochondria-mediated reactive oxygen species (ROS) accumulation. Adapted from [62].
Figure 7
Figure 7
Overview of microglial functions in response to stress and AD pathology. Adapted from [71].
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This research received no external funding.